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(Circulation. 1998;98:435-440.)
© 1998 American Heart Association, Inc.

Clinical Investigation and Reports

Increased QT Dispersion in Patients With Vasospastic Angina

Makoto Suzuki, MD; Mitsuhiro Nishizaki, MD; Masataka Arita, MD; Takashi Ashikaga, MD; Noriyoshi Yamawake, MD; Tsunekazu Kakuta, MD; Fujio Numano, MD; ; Masayasu Hiraoka, MD

From the Department of Cardiology, Yokohama Minami Kyosai Hospital, Yokohama, Japan (M.S., M.N., M.A., T.A., N.Y.); the Third Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo, Japan (T.K., F.N.); and the Department of Cardiovascular Diseases, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan (M.H.).

Correspondence to Mitsuhiro Nishizaki, MD, Department of Cardiology, Yokohama Minami Kyosai Hospital, 500, Mutsuura, Kanazawa-ku, Yokohama, Kanagawa, 236-0031, Japan.

Background—The risk factors for ventricular arrhythmias in patients with coronary vasospasm have not been identified. We evaluated QT dispersion in patients with vasospastic angina and its relation to susceptibility to ventricular arrhythmias during myocardial ischemia and reperfusion.

Methods and Results—We assessed the corrected QT (QTc) dispersion before induction of coronary artery spasm by intracoronary injection of acetylcholine (baseline) and 30 minutes after administration of isosorbide dinitrate in 50 patients with vasospastic angina and 50 patients with atypical chest pain. The baseline QTc dispersion was significantly greater in patients with vasospastic angina than in patients with atypical chest pain (mean±SD: 69±24 versus 44±19 ms, 95% confidence interval of mean difference [CI]: 16 to 33 ms; P<0.001). QTc dispersion decreased significantly, to 48±15 ms (CI: 15 to 26 ms; P<0.001 versus baseline), after administration of isosorbide dinitrate in patients with vasospastic angina but did not change significantly in patients with atypical chest pain (mean±SD: 41±17 ms, CI: -3 to 9 ms). During the provocation test, 24 of 50 patients with vasospastic angina experienced ventricular arrhythmias. The baseline QTc dispersion was significantly greater in patients with than without ventricular arrhythmias (mean±SD: 77±23 versus 61±19 ms, CI: 4 to 26 ms; P<0.05).

Conclusions—Patients with vasospastic angina exhibited an increased baseline QTc dispersion compared with patients with atypical chest pain, which suggests that inhomogeneity of repolarization and susceptibility to ventricular arrhythmias are increased in patients with vasospastic angina, even when asymptomatic. The association between increased QTc dispersion and ventricular arrhythmias during the provocation test suggests that measurement of QT dispersion may help predict which patients with vasospastic angina are at high risk for ventricular arrhythmias during ischemia.

Key Words: angina • vasospasm • intervals • arrhythmia • death, sudden

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